ライフサイエンスコーパス: insulin-resistant

1 i) quartiles: Q1 = more sensitive; Q4 = more insulin resistant).

2 ivity) or a high-fat diet (HFD; for 2 weeks, insulin-resistant).

3 d-type mice administered recombinant CRP are insulin resistant.

4 pose tissue that for unknown reasons becomes insulin resistant.

5 obese, hyperphagic, glucose intolerant, and insulin resistant.

6 atients had increased abdominal fat and were insulin resistant.

7 in which the liver appears to be selectively insulin resistant.

8 d pancreatic beta-cell activity and are more insulin resistant.

9 They were not, however, insulin resistant.

10 NPLA3 genotypes, but the obese subjects were insulin-resistant.

11 in high-fat diet-fed mice that are obese and insulin-resistant.

12 nce tests showed that male Znt7 KO mice were insulin-resistant.

13 ted comorbidities in obese children, who are insulin-resistant.

14 ent was started in female Zucker fatty rats (insulin resistant) 1 week before carotid artery balloon

15 several insulin resistance models, including insulin-resistant 3T3-L1 adipocytes and fat explants pre

16 elease of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, ca

17 ATP stimulated 2-NBDG uptake in normal and insulin-resistant adult muscle fibers, resembling the re

18 adipose tissue lipolysis or inflammation in insulin-resistant adults.

19 2) with a placebo (4.2 g oleate/d; n = 9) in insulin-resistant adults.

20 of which subjects would be considered to be insulin resistant after 6 mo of weight maintenance [vali

21 drenergic receptor activation, and were more insulin resistant after a high-fat diet challenge.

22 ment showed that the TRPV1 KO mice were more insulin resistant after HFD because of the approximately

23 airments in AS160 phosphorylation evident in insulin-resistant aged individuals.

24 quires unsuppressible hyperglucagonemia from insulin-resistant alpha cells and is prevented by glucag

25 on of Akt1 and Akt2 were glucose intolerant, insulin resistant and defective in their transcriptional

26 ive stress and inflammation were elevated in insulin resistant and diabetic rats.

27 RBP4-overexpressing mice (RBP4-Ox) are insulin resistant and glucose intolerant and have increa

28 Although lean female MKR mice are insulin resistant and glucose intolerant, displaying acc

29 e with those in YL, whereas OO were markedly insulin resistant and had more than twofold greater IMCL

30 677 NW individuals (20%) were classified as insulin resistant and normal weight (IR-NW), and 72 of 3

31 ng of mice exposed to HFD during IU/L became insulin resistant and obese and exhibited increased adip

32 osen for extremes of insulin sensitivity (31 insulin-resistant and 31 insulin-sensitive subjects; 40

33 d compared between ethnic groups and between insulin-resistant and insulin-sensitive participants ind

34 HPAH animal models are insulin resistant, and cells with BMPR2 mutation have im

35 urn-injured adults remain hyperglycemic, are insulin resistant, and express defects in insulin secret

36 summary, BG4KO mice are glucose intolerant, insulin resistant, and have impaired glucose sensing, in

37 ushingoid and by 21 weeks of age were obese, insulin-resistant, and had extensive areas of hepatic ge

38 female mutant mice were glucose intolerant, insulin-resistant, and hyperglycemic, and these metaboli

39 The diabetic CPCs were insulin-resistant, and they showed higher energetic reli

40 ids were determined among insulin-sensitive, insulin-resistant, and type 2 diabetic (T2DM) individual

41 from insulin-sensitive animals but not from insulin-resistant animals.

42 without steatosis, patients with NAFLD were insulin resistant at the level of adipose tissue, liver,

43 Reduced inflammation in obese/insulin resistant B cell-null mice associates with an in

44 All patients were insulin resistant based on a Homeostasis Model Assessmen

45 Here we show that LIRKO mice are severely insulin resistant based on glucose, insulin and C-peptid

46 ng and glucose-lowering pathways that become insulin-resistant but also lipogenic pathways that remai

47 Hearts of rats, rendered insulin resistant by high-sucrose feeding, were subjecte

48 Male adult Sprague-Dawley rats were rendered insulin-resistant by feeding high fat diet for 16 weeks.

49 In vivo administration of these compounds to insulin resistant C57Bl/6J mice fed a high fat diet redu

50 ely downregulated in adipose tissue of obese insulin-resistant C57BL/6J mice and in human obesity-lin

51 sue is an important etiological component in insulin-resistant cardiometabolic disease and highlight

52 hibits PTP and improves IFNalpha response in insulin-resistant cells.

53 verely obese (mean BMI 34.6 +/- 6.6 kg/m(2)) insulin-resistant children aged 6-12 years, randomized t

54 omposition, and glucose homeostasis in obese insulin-resistant children participating in a low-intens

55 This effect was attenuated in insulin-resistant cohorts, both those with IGT and those

56 Type 1 diabetic patients are insulin resistant compared with nondiabetic subjects, an

57 found to be upregulated in the intestine of insulin-resistant compared to insulin-sensitive subjects

58 nd differently expressed in the intestine of insulin-resistant compared to insulin-sensitive subjects

59 ht, body fat mass, fasting glucose, and were insulin-resistant compared with chow mice.

60 factor/receptor expression were unchanged in insulin-resistant compared with control mice, indicating

61 te the effect of insulin to modulate GSIS in insulin-resistant compared with insulin-sensitive subjec

62 e heart and metabolic parameters under obese-insulin resistant condition is not known.

63 ity may contribute to anabolic resistance in insulin-resistant conditions by impairing translation in

64 Under insulin-resistant conditions such as obesity, pancreatic

65 take in response to exercise is preserved in insulin-resistant conditions, but the signals involved a

66 Under insulin-resistant conditions, it is well known that insu

67 eletal muscle mass appears to be impaired in insulin-resistant conditions, such as type 2 diabetes, t

68 Adipose tissue inflammation is present in insulin-resistant conditions.

69 ole in altered hepatic apoB100 metabolism in insulin-resistant conditions.

70 that the brain of aged APP/PS1 mice was not insulin resistant, contrary to the current state of the

71 trations and improved insulin sensitivity in insulin-resistant db/db mice, our results suggest that c

72 imizing ectopic fat accumulation that causes insulin-resistant diabetes and non-alcoholic fatty liver

73 db/db mice, a widely used model of insulin-resistant diabetes and obesity, were either pair

74 the development of systemic inflammation and insulin-resistant diabetes mellitus type 2 (DM).

75 efore be therapeutically useful for treating insulin-resistant diabetes.

76 decreased in mice with insulin-deficient or insulin-resistant diabetes.

77 in humans and experimental animal models of insulin-resistant diabetes.

78 protected mice from diet-induced obesity and insulin-resistant diabetes.

79 ding cause of death of patients with type 2 (insulin-resistant) diabetes.

80 The livers of insulin-resistant, diabetic mice manifest selective insu

81 deficiency, glucose transporter aberrations, insulin-resistant diabetogenic responses, and distinct c

82 In addition, apoA-I injections in insulin-resistant diet-induced obese (DIO) mice lead to

83 ds were investigated in diabetic db/db mice, insulin-resistant diet-induced obese (DIO) mice, and rat

84 d with a 40% fat diet, they become obese and insulin resistant, display increased serum cytokine leve

85 sk factor for T2DM, most individuals who are insulin resistant do not develop diabetes.

86 e cells, independent of donor Si, cells from insulin-resistant donors show markedly impaired GSV teth

87 strate-1 (IRS1-het) are hyperinsulinemic and insulin resistant during pregnancy, despite normal plasm

88 in association with basal hyperinsulinemia, insulin-resistant endogenous glucose production, and dow

89 of Nox2, which was specifically elevated in insulin-resistant endothelial cells, significantly reduc

90 demonstrated higher levels of superoxide in insulin-resistant endothelial cells, which could be phar

91 ranscriptome sequencing (RNA-seq) studies in insulin-resistant fat bodies revealed differential expre

92 it, with glucose uptake enhancing ability in insulin-resistant FL83B mouse hepatocytes, as shown in o

93 nd other genes distinguish adipose tissue of insulin resistant from insulin-sensitive individuals wit

94 noid receptor, appears to be up-regulated in insulin-resistant, glucose-intolerant mice.

95 mass index (BMI; in kg/m(2)): 23.2 +/- 1.5]; insulin-resistant, glucose-tolerant, obese humans (OBEs)

96 altered beta-cell-to-alpha-cell area in the insulin- resistant group.

97 vere obesity were compared indicate that the insulin-resistant group is also distinguished by increas

98 ed muscles from the insulin-sensitive versus insulin-resistant group.

99 Interestingly, fructose-fed, insulin-resistant hamsters showed a more pronounced resp

100 ty and increases virologic response rates in insulin-resistant HCV genotype 4 patients, but it is unc

101 an be manipulated to improve function of the insulin-resistant heart.

102 escue constrained glucose utilization in the insulin-resistant heart.

103 lating substrate uptake and oxidation in the insulin-resistant heart.

104 s from chow-fed rats recovered to 93%, while insulin-resistant hearts recovered only to 80% (P<0.001

105 We hypothesized that by forming insulin-resistant heterodimers composed of one IGF-1Ralp

106 sed the function of CD11c-positive ATMs when insulin resistant high fat diet (HFD) mice become insuli

107 In this study, we show that in insulin-resistant high-fat diet-fed mice, the enhanced i

108 mined insulin signaling factors in brains of insulin-resistant high-fat-fed mice, ob/ob mice, mice wi

109 f insulin-sensitive (HOMA-IR < 3, n = 9) and insulin-resistant (HOMA-IR > 7, n = 9) obese subjects we

110 decreased and PTEN activity is increased in insulin-resistant human subjects.

111 te that plasma betaine levels are reduced in insulin-resistant humans and correlate closely with insu

112 capillaries, and reduced MCP-1 expression in insulin-resistant humans and in macrophages and adipocyt

113 valine) are elevated in the blood of obese, insulin-resistant humans and rodents.

114 ios are increased in serum of lean and obese insulin-resistant humans compared to ratios in insulin-s

115 ransiently upregulated in the liver of obese insulin-resistant humans with or without fatty liver, gi

116 sphorus metabolites in insulin-sensitive and insulin-resistant humans.

117 d are reduced in adipose tissue and serum of insulin-resistant humans.

118 ation enzymes in adipose tissue in obese and insulin-resistant humans.

119 n resistant male mice and increased in obese/insulin-resistant humans.

120 lipid-overloaded hypertrophic adipocytes are insulin resistant independent of adipocyte inflammation.

121 We studied 12 healthy, young, lean, insulin resistant individuals in an interventional, rand

122 atherogenic dyslipidemia and NAFLD in young insulin resistant individuals who are prone to develop t

123 levels in muscle, fat, and skin tissues from insulin resistant individuals, but similar data on liver

124 f insulin-sensitive individuals and those of insulin-resistant individuals (matched on BMI), trans-re

125 aring fat oxidation in insulin-sensitive and insulin-resistant individuals have shown that fat oxidat

126 indicating that the mitochondrial defect in insulin-resistant individuals is, at least in part, reve

127 idation is higher in T2DM patients and obese insulin-resistant individuals than in insulin-sensitive

128 patients with type 2 diabetes (T2DM), obese insulin-resistant individuals, and lean insulin-resistan

129 bolic syndrome, showing that in lean, young, insulin-resistant individuals, impaired muscle glucose t

130 r the upregulation of triglyceride levels in insulin-resistant individuals, in addition to identifyin

131 patic fatty acid oxidation is upregulated in insulin-resistant individuals.

132 In an insulin resistant, insulinopenic model of diabetes, XMet

133 d PAK activation was decreased in both acute insulin-resistant (intralipid infusion) and chronic insu

134 Insulin-resistant iPSC also showed reduced catalase acti

135 Insulin-resistant iPSC had increased mitochondrial numbe

136 proliferation were also potently reduced in insulin resistant iPSCs.

137 analysis revealed marked differences in both insulin-resistant iPSCs and corresponding fibroblasts co

138 yzed muscle biopsy samples from young, lean, insulin resistant (IR) offspring of parents with type 2

139 weight/obese individuals classified as IS or insulin resistant (IR).

140 egnant females on HF diet were segregated as insulin resistant (IR; HF+IR) or insulin sensitive (IS;

141 sified as insulin-sensitive [IS] [n = 64] or insulin-resistant [IR] [n = 79] by euglycemic clamp) rec

142 trial registry: TAYSIDE trial (Metformin in Insulin Resistant Left Ventricular [LV] Dysfunction).

143 ipants is 2- and 3-fold greater than in lean insulin-resistant (LIR) and obese insulin-resistant (OIR

144 FoxO6 becomes deregulated in the insulin-resistant liver, accounting for its unbridled ac

145 ereby preventing the transformation into the insulin-resistant liver.

146 emoattractant protein-1 and VCAM-1 levels in insulin-resistant LMCs indicated activation of inflammat

147 ymphatic muscle contraction, was observed in insulin-resistant LMCs.

148 ession of SIRT1 in the liver of diet-induced insulin-resistant low-density lipoprotein receptor-defic

149 OBEs and T2Ds were similarly insulin resistant (M value: 3.5 +/- 1.4 and 1.9 +/- 2.5

150 protein kinase A thus offers a way to rescue insulin-resistant macrophages from excessive ER stress r

151 eversed the increase in UPR and apoptosis of insulin-resistant macrophages in atherosclerotic lesions

152 element-binding protein (CREBP) signaling in insulin-resistant macrophages leads to decreased express

153 to free cholesterol or oxysterol loading in insulin-resistant macrophages.

154 ssed by insulin in vitro, increased in obese/insulin resistant male mice and increased in obese/insul

155 n glucose transport in insulin-sensitive and insulin-resistant mature skeletal muscle has not previou

156 d that youths with type 1 diabetes were more insulin resistant (median glucose infusion rate 10.1 vs.

157 -designed randomized controlled trial in 121 insulin-resistant men and women, we measured vascular fu

158 ingle-blind, randomized, crossover study, 10 insulin-resistant men consumed 3 high-fat mixed meals (2

159 es involved in lipid metabolism in 28 obese, insulin-resistant men.

160 d postprandial insulin sensitivity in obese, insulin-resistant men.

161 and of Sirt2 activators in the treatment of insulin-resistant metabolic disorders.

162 rison of the effects of hyperglycemic and/or insulin-resistant metabolic stress conditions on human a

163 Insulin-resistant MetS subjects with more metabolic comp

164 Insulin-resistant MetS subjects with the highest HOMA-IR

165 urthermore, C22:1-CoA was 2.3-fold higher in insulin-resistant mice and correlated significantly with

166 and signaling were investigated in muscle of insulin-resistant mice and humans.

167 ered in liver of both ob/ob and diet-induced insulin-resistant mice and improved by rosiglitazone tre

168 insulin in normal mice, increased basally in insulin-resistant mice and monkeys, and accompanied by d

169 bd2 was down-regulated in diet-induced obese insulin-resistant mice in a leptin-dependent manner.

170 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.

171 Skeletal muscle from insulin-resistant mice recapitulated this gene expressio

172 Knockdown of FMO3 in insulin-resistant mice suppresses FoxO1, a central node

173 by promoting complete lipid use in muscle of insulin-resistant mice through mitochondrial biogenesis

174 High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0

175 Here, we report that treatment of obese insulin-resistant mice with an allosteric MK2/3 inhibito

176 tissue of ob/ob mice and diet-induced obese, insulin-resistant mice.

177 lates growth of pancreatic beta cell mass in insulin-resistant mice.

178 e tolerance and insulin sensitivity in obese insulin-resistant mice.

179 vo administration in lean mice and in obese, insulin-resistant mice.

180 hosphorylation in cultured adipocytes and in insulin-resistant mice.

181 in skeletal muscle of diet induced obese and insulin resistant mouse models we generated mice express

182 naling is inappropriately activated in obese/insulin-resistant mouse models.

183 use mechanisms for exercise effects on GU in insulin-resistant muscle are unknown, our primary object

184 al insulin sensitivity and glucose uptake in insulin-resistant muscle cells, and this effect was depe

185 ucose uptake additively with insulin, and in insulin-resistant muscle, and alters the phosphorylation

186 ulin-sensitive muscle, in the basal state in insulin-resistant muscle, and if so, to determine whethe

187 In insulin-resistant muscle, caCaMKKalpha increased basal g

188 t target the vasculature in the treatment of insulin-resistant muscle.

189 vary in their properties between healthy and insulin-resistant muscle.

190 n mitochondrial protein abundance present in insulin-resistant muscle.

191 t alternative to stimulate glucose uptake in insulin-resistant muscle.

192 rotein, and phosphorylation are increased in insulin-resistant muscles.

193 m lean healthy control subjects (LCs), obese insulin-resistant nondiabetic control subjects (OCs), an

194 Insulin-resistant, nondiabetic subjects were treated wit

195 ta on the prognosis of insulin-sensitive and insulin-resistant normal-weight (NW) or obese individual

196 upported by our finding that in the severely insulin resistant ob/ob mouse strain a DNA-binding-defec

197 Primary macrophages from insulin-resistant ob/ob and insulin receptor (Insr)(-/-)

198 Insulin-resistant ob/ob mice have increased PTP-1B gene

199 icient to lower glucose levels in normal and insulin-resistant ob/ob mice, without altering insulin o

200 diet-induced obese and genetically obese and insulin-resistant ob/ob mice.

201 n adipose tissue from metabolically abnormal insulin-resistant obese (MAO) subjects, metabolically no

202 imately 23 years) insulin-sensitive lean and insulin-resistant obese men and women were studied.

203 he response to IFNalpha was also measured in insulin-resistant obese mice (high fat diet and ob/ob mi

204 ctivity and improves response to IFNalpha in insulin-resistant obese mice.

205 Ceramide content was higher in insulin-resistant obese muscle.

206 insulin resistance were observed in healthy insulin-resistant obese subjects and obese type 2 diabet

207 y, in matched biopsies from "healthy" versus insulin-resistant obese subjects we find HO-1 to be amon

208 bese insulin-resistant individuals, and lean insulin-resistant offspring of parents with T2DM have ~3

209 e insulin resistance in healthy, young, lean insulin-resistant offspring of parents with type 2 diabe

210 an in lean insulin-resistant (LIR) and obese insulin-resistant (OIR) participants, respectively.

211 denectomy from nondiabetic subjects who were insulin-resistant or insulin-sensitive.

212 The downstream mediators of insulin-resistant pathophysiology remain unclear.

213 Sequencing of ARL15 in 375 severely insulin resistant patients identified four rare heterozy

214 ges during an 8-wk LCD allowed us to predict insulin-resistant patients after 6 mo of weight maintena

215 insufficient to maintain protein balance in insulin-resistant patients during tight glucose control.

216 Among insulin-resistant patients with a recent ischaemic strok

217 In obese, insulin-resistant patients with nonalcoholic fatty liver

218 hich adipose tissue of insulin-sensitive and insulin-resistant patients with severe obesity were comp

219 In chronically insulin-resistant patients with T2DM, hyperglycemic-hype

220 g in 13 normal subjects and in 6 chronically insulin-resistant patients with type 2 diabetes mellitus

221 months after RDN treatment in this group of insulin-resistant patients without diabetes and with res

222 a, a common pancreatic disorder in obese and insulin-resistant patients, is known to cause amylin oli

223 nce exercise improves insulin sensitivity in insulin-resistant patients, we hypothesized that it woul

224 hinery, is dramatically altered in obese and insulin-resistant patients.

225 PAHSA levels are reduced in insulin resistant people, and levels correlate highly wi

226 ulin secretion (GSIS) would be diminished in insulin-resistant persons.

227 -dependent activation of PKCtheta induces an insulin-resistant phenotype, limiting the access of tumo

228 sult in transgenerational inheritance of the insulin-resistant phenotype.

229 disorders and directing adipocytes to a more insulin-resistant phenotype.

230 pid free radical overproduction exists in an insulin-resistant rat model and that reducing the accumu

231 us muscle of high sucrose diet (HSD) induced insulin resistant rats and TNF-alpha exposed cultured my

232 at VNS attenuates cognitive decline in obese-insulin resistant rats by attenuating brain mitochondria

233 and EPC survival is impaired in Zucker fatty insulin resistant rats.

234 rved cardiac mitochondrial function in obese-insulin resistant rats.

235 e variability (HRV) and LV function in obese-insulin resistant rats.

236 genetic model of spontaneously hypertensive, insulin-resistant rats (SHHF).

237 its target genes was enhanced in nondiabetic insulin-resistant rats and markedly reduced with diabete

238 High-fat diet (HFD)-fed, insulin-resistant rats show attenuated angiotensin (ANG)

239 EPCs from Zucker fatty insulin-resistant rats were cultured and exposed to tumo

240 were performed in normal rats, high fat-fed insulin-resistant rats, and insulin receptor 2'-O-methox

241 retina and systemic circulation of obese and insulin resistant rodents with and without diabetes.

242 e of human subjects with type-2 diabetes and insulin resistant rodents.

243 f lipolysis, whereas obese-derived ASCs were insulin-resistant, showing impaired insulin-stimulated g

244 hat 1) HA content is increased in the ECM of insulin-resistant skeletal muscle and 2) reduction of HA

245 rate many of the defects observed in vivo in insulin-resistant skeletal muscle and provide a new mode

246 normal oxidative capacity of mitochondria in insulin-resistant skeletal muscle in parallel with high

247 trix (ECM) components is a characteristic of insulin-resistant skeletal muscle.

248 control and insulin sensitivity in the obese insulin resistant state.

249 otes compensatory beta-cell expansion in the insulin-resistant state and in response to beta-cell str

250 ffects and mechanisms of action in the obese insulin-resistant state are unknown.

251 Obesity induces an insulin-resistant state in adipose tissue, liver, and mu

252 Sleep restriction results in an insulin-resistant state in human adipocytes.

253 The obese insulin-resistant state is characterized by impairments

254 Baf60c in glucose homeostasis in the severe insulin-resistant state remain unknown.

255 h to identify biomarkers of diabetes and the insulin-resistant state that precedes overt pathology.

256 rugs might accelerate the transition from an insulin-resistant state to overt diabetes.

257 ir wild type controls at 4 months of age (an insulin-resistant state) versus a 5-fold difference betw

258 IMCD could contribute to hypertension in the insulin-resistant state.

259 In insulin resistant states such as type 2 diabetes, there

260 -resistant (intralipid infusion) and chronic insulin-resistant states (obesity and diabetes).

261 ction by insulin is consistently abnormal in insulin-resistant states and diabetes.

262 a seen in common metabolic disorders such as insulin-resistant states and type 2 diabetes and likely

263 Obese, insulin-resistant states are characterized by a paradoxi

264 its levels are also abnormally increased in insulin-resistant states in rodents and humans.

265 treatment of type 2 diabetes and other human insulin-resistant states in the future.

266 ies that increase the cardiovascular risk in insulin-resistant states of obesity, MetSyn and T2DM.

267 Moreover, insulin-resistant states such as type 2 diabetes mellitu

268 ptor in the proximal tubule, which occurs in insulin-resistant states, may promote hyperglycemia thro

269 to the development of hyperproinsulinemia in insulin-resistant states.

270 preserves WAT lipid homeostasis in obese and insulin-resistant states.

271 us impacts energy homeostasis in obesity and insulin-resistant states.

272 uman skeletal muscle and are dysregulated in insulin-resistant states.

273 l function, apoptosis and cognition in obese-insulin resistant subjects have never been investigated.

274 ably, in humans, we show that both obese and insulin-resistant subjects have elevated plasma concentr

275 ates glucose-stimulated insulin secretion in insulin-resistant subjects to a lesser degree than in no

276 es from patients with T2D; normoglycemic but insulin-resistant subjects with a parental family histor

277 n improves insulin signalling in muscle from insulin-resistant subjects.

278 unting for a mild increase of iron stores in insulin-resistant subjects.

279 redicted to be activated in the intestine of insulin-resistant subjects.

280 viously identified in the intestine of obese insulin-resistant subjects.

281 ts of MHC-PDK4 mice were shown to exhibit an insulin-resistant substrate utilization profile, charact

282 ed ATP synthesis) also has been described in insulin-resistant T2DM and obese subjects.

283 d postexercise ATP resynthesis and were more insulin resistant than control subjects.

284 d that the TRPV1 KO mice were more obese and insulin resistant than the WT mice at 9 mo of age.

285 xposure, while APNko-DHT mice were even more insulin resistant than their DHT-exposed littermate WTs.

286 Migrant south Asians seem to be more insulin resistant than white Europeans across the life c

287 Although both strains were equally insulin resistant, the MUP-uPA mice exhibited more liver

288 Insulin-resistant type 2 diabetes mellitus is associated

289 d in macrophages from db/db and diet-induced insulin-resistant type 2 diabetic (T2D) mice, but not fr

290 e expression showed more differences between insulin-resistant versus insulin-sensitive groups than t

291 n (TNMD) is upregulated in adipose tissue of insulin-resistant versus insulin-sensitive individuals,

292 jects and further stratified the cohort into insulin-resistant versus insulin-sensitive subgroups bas

293 sease, patients with advanced NASH were more insulin-resistant, viscerally obese, and older, but ther

294 However, not all obese individuals are insulin resistant, which confounds our understanding of

295 on-alcoholic fatty liver disease and who are insulin resistant, will be randomised into either a Medi

296 bal androgen receptor (AR) knockout mice are insulin resistant with increased fat, but it is unclear

297 n non-haematopoietic tissue become obese and insulin resistant with loss of Epo regulation of energy

298 e determined whether obese (BMI 33 kg/m(2)), insulin-resistant women with polycystic ovary syndrome h

299 show that duodenal bypass surgery on obese, insulin-resistant Zucker fa/fa rats restored insulin sen

300 p-Tyr911 of IRS2 were observed in vessels of insulin-resistant Zucker fatty rats versus lean rats.